Chromatid Cohesion (chromatid + cohesion)

Distribution by Scientific Domains
Life Sciences88%

Kinds of Chromatid Cohesion

  • sister chromatid cohesion
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    Selected Abstracts

    Cloning of Xenopus orthologs of Ctf7/Eco1 acetyltransferase and initial characterization of XEco2

    FEBS JOURNAL, Issue 24 2008
    Masatoshi Takagi
    Sister chromatid cohesion is important for the correct alignment and segregation of chromosomes during cell division. Although the cohesin complex has been shown to play a physical role in holding sister chromatids together, its loading onto chromatin is not sufficient for the establishment of sister chromatid cohesion. The activity of the cohesin complex must be turned on by Ctf7/Eco1 acetyltransferase at the replication forks as the result of a specific mechanism. To dissect this mechanism in the well established in vitro system based on the use of Xenopus egg extracts, we cloned two Xenopus orthologs of Ctf7/Eco1 acetyltransferase, XEco1 and XEco2. Both proteins share a domain structure with known members of Ctf7/Eco1 family proteins. Moreover, biochemical analysis showed that XEco2 exhibited acetyltransferase activity. We raised a specific antibody against XEco2 and used it to further characterize XEco2. In tissue culture cells, XEco2 gradually accumulated in nuclei through the S phase. In nuclei formed in egg extract, XEco2 was loaded into the chromatin at a constant level in a manner sensitive to geminin, an inhibitor of the pre-replication complex assembly, but insensitive to aphidicolin, an inhibitor of DNA polymerases. In both systems, no specific localization was observed during mitosis. In XEco2-depleted egg extracts, DNA replication occurred with normal kinetics and efficiency, and the condensation and sister chromatid cohesion of subsequently formed mitotic chromosomes was unaffected. These observations will serve as a platform for elucidating the molecular function of Ctf7/Eco1 acetyltransferase in the establishment of sister chromatid cohesion in future studies, in which XEco1 and XEco2 should be dissected in parallel. [source]

    Sister chromatid cohesion: the cohesin cleavage model does not ring true

    GENES TO CELLS, Issue 6 2007
    Vincent Guacci
    Sister chromatid cohesion is important for high fidelity chromosome segregation during anaphase. Gene products that provide structural components (cohesin complex or cohesin) and regulatory components responsible for cohesion are conserved through eukaryotes. A simple model where cohesion establishment occurs by replication through static cohesin rings and cohesion dissolution occurs by Esp1p/separase mediated cleavage of the cohesin rings (Mcd1p/Rad21p/Scc1p sub-unit cleavage) has become widespread. A growing body of evidence is inconsistent with this ring cleavage model. This review will summarize the evidence showing that cohesin complex is not static but is regulated at multiple cell cycle stages before anaphase in a separase independent manner. Separase is indeed required at anaphase for complete chromosome segregation. However, multiple mechanisms for cohesion dissolution appear to act concurrently during anaphase. Separase is only one such mechanism and its importance varies from organism to organism. The idea that cohesin is a dynamic complex subjected to regulation at various cell cycle stages by multiple mechanisms makes sense in light of the myriad functions in which it has been implicated, such as DNA damage repair, gene silencing and chromosome condensation. [source]

    Cell cycle execution point analysis of ORC function and characterization of the checkpoint response to ORC inactivation in Saccharomyces cerevisiae

    GENES TO CELLS, Issue 6 2006
    Daniel G. Gibson
    Chromosomal replication initiates through the assembly of a prereplicative complex (pre-RC) at individual replication origins in the G1-phase, followed by activation of these complexes in the S-phase. In Saccharomyces cerevisiae, the origin recognition complex (ORC) binds replication origins throughout the cell cycle and participates in pre-RC assembly. Whether the ORC plays an additional role subsequent to pre-RC assembly in replication initiation or any other essential cell cycle process is not clear. To study the function of the ORC during defined cell cycle periods, we performed cell cycle execution point analyses with strains containing a conditional mutation in the ORC1, ORC2 or ORC5 subunit of ORC. We found that the ORC is essential for replication initiation, but is dispensable for replication elongation or later cell cycle events. Defective initiation in ORC mutant cells results in incomplete replication and mitotic arrest enforced by the DNA damage and spindle assembly checkpoint pathways. The involvement of the spindle assembly checkpoint implies a defect in kinetochore-spindle attachment or sister chromatid cohesion due to incomplete replication and/or DNA damage. Remarkably, under semipermissive conditions for ORC1 function, the spindle checkpoint alone suffices to block proliferation, suggesting this checkpoint is highly sensitive to replication initiation defects. We discuss the potential significance of these overlapping checkpoints and the impact of our findings on previously postulated role(s) of ORCs in other cell cycle functions. [source]

    SMC Proteins at the Crossroads of Diverse Chromosomal Processes

    IUBMB LIFE, Issue 12 2003
    Rolf Jessberger
    Abstract How should a protein be designed to serve in processes as diverse as chromosome condensation, sister chromatid cohesion, DNA recombination, gene dosage regulation, and perhaps even gene silencing or transcriptional regulation - which occur in both mitosis and meiosis? Such a protein or protein complex needs to bear DNA interaction domains, it needs the capacity to use energy to move DNA, it needs to enter into highly specific protein interactions, it needs to be large enough to link two DNA molecules, it needs to be of sufficient flexibility to cope with different types of chromatin structure, yet it also needs to be rigid enough to pull, push or enclose DNA. SMC proteins fulfill these requirements and form the core units of high molecular weight complexes that act in all those processes, and are essential for some of them. SMC stands for 'Structural Maintenance of Chromosomes', although SMC proteins are not static scaffold proteins merely providing support for a particular chromosome structure. SMC proteins are rather highly dynamic actors, that generate and modulate chromosome structures, affecting a plethora of biological processes. IUBMB Life, 55: 643-652, 2003 [source]

    Sexual devolution in plants: apomixis uncloaked?

    BIOESSAYS, Issue 9 2008
    Richard D. Noyes
    There are a growing number of examples where naturally occurring mutations disrupt an established physiological or developmental pathway to yield a new condition that is evolutionary favored. Asexual reproduction by seed in plants, or apomixis, occurs in a diversity of taxa and has evolved from sexual ancestors. One form of apomixis, diplospory, is a multi-step development process that is initiated when meiosis is altered to produce an unreduced rather than a reduced egg cell. Subsequent parthenogenetic development of the unreduced egg yields genetically maternal progeny. While it has long been apparent from cytological data that meiosis in apomicts was malfunctional or completely bypassed, the genetic basis of the phenomenon has been a long-standing mystery. New data from genetic analysis of Arabidopsis mutants1 in combination with more sophisticated molecular understanding of meiosis in plants indicate that a weak mutation of the gene SWI, called DYAD, interferes with sister chromatid cohesion in meiosis I, causes synapsis to fail in female meiosis and yields two unreduced cells. The new work shows that a low percentage of DYAD ovules produce functional unreduced egg cells (2n) that can be fertilized by haploid pollen (1n) to give rise to triploid (3n) progeny. While the DYAD mutants differ in some aspects from naturally occurring apomicts, the work establishes that mutation to a single gene can effectively initiate apomictic development and, furthermore, focuses efforts to isolate apomixis genes on a narrowed set of developmental events. Profitable manipulation of meiosis and recombination in agronomically important crops may be on the horizon. BioEssays 30:798,801, 2008. © 2008 Wiley Periodicals, Inc. [source]

    Cohesin and CTCF: cooperating to control chromosome conformation?

    BIOESSAYS, Issue 8 2008
    Maria Gause
    The cohesin complex is best known for its role in sister chromatid cohesion. Over the past few years, it has become apparent that cohesin also regulates gene expression, but the mechanisms by which it does so are unknown. Recently, three groups mapped numerous cohesin-binding sites in mammalian chromosomes and found substantial overlap with the CCCTC-binding factor (CTCF).1,3 CTCF is an insulator protein that blocks enhancer,promoter interactions, and the investigators found that cohesin also contributes to this activity. Thus, these studies demonstrate at least one mechanism by which cohesin can control gene expression. BioEssays 30:715,718, 2008. © 2008 Wiley Periodicals, Inc. [source]

    Shugoshin: a centromeric guardian senses tension

    BIOESSAYS, Issue 6 2005
    Sarah E. Goulding
    To ensure accurate chromosome segregation during mitosis, the spindle checkpoint monitors chromosome alignment on the mitotic spindle. Indjeian and colleagues have investigated the precise role of the shugoshin 1 protein (Sgo1p) in this process in budding yeast.1 The Sgo proteins were originally identified as highly conserved proteins that protect cohesion at centromeres during the first meiotic division. Together with other recent findings,2 the study highlighted here has identified Sgo1 as a component that informs the mitotic spindle checkpoint when spindle tension is perturbed. This discovery has provided a molecular link between sister chromatid cohesion and tension-sensing at the kinetochore,microtubule interface. BioEssays 27:588,591, 2005. © 2005 Wiley Periodicals, Inc. [source]

    Cornelia de Lange syndrome, cohesin, and beyond

    CLINICAL GENETICS, Issue 4 2009
    J Liu
    Cornelia de Lange syndrome (CdLS) (OMIM #122470, #300590 and #610759) is a dominant genetic disorder with multiple organ system abnormalities which is classically characterized by typical facial features, growth and mental retardation, upper limb defects, hirsutism, gastrointestinal and other visceral system involvement. Mutations in three cohesin proteins, a key regulator of cohesin, NIPBL, and two structural components of the cohesin ring SMC1A and SMC3, etiologically account for about 65% of individuals with CdLS. Cohesin controls faithful chromosome segregation during the mitotic and meiotic cell cycles. Multiple proteins in the cohesin pathway are also involved in additional fundamental biological events such as double-strand DNA break repair and long-range regulation of transcription. Moreover, chromosome instability was recently associated with defective sister chromatid cohesion in several cancer studies, and an increasing number of human developmental disorders is being reported to result from disruption of this pathway. Here, we will discuss the human disorders caused by alterations of cohesin function (termed ,cohesinopathies'), with an emphasis on the clinical manifestations of CdLS and mechanistic studies of the CdLS-related proteins. [source]